Unlike Heparin, Low-Molecular Weight Heparin Does Not Suppress Aldosterone Production

Jm, Marcelli; Jd, Lalau; Abourachid, H; Jc, Quiret; Quichaud, J

doi:10.1055/s-2007-1009248

Cited by 10 publications

(5 citation statements)

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“…4,6,7 However, such effect was not demonstrated in all studies. 8 We did not find a decrease in aldosterone levels in our study. Moreover, a trend towards elevation of rennin activity and aldosterone levels, as well as a significant increase in potassium levels during the study period were observed.…”

Section: Discussioncontrasting

confidence: 70%

Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study

Koren‐Michowitz

Avni

Michowitz

et al. 2003

Pharmacoepidemiology and Drug

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Section: Discussioncontrasting

confidence: 70%

Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study

Koren‐Michowitz

Avni

Michowitz

et al. 2003

Pharmacoepidemiology and Drug

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“…Although previous reports have shown LMWH therapy to increase serum potassium concentration [6,7], others failed to show similar results [8]. Conflicting data regarding the effect of LMWH on aldosterone secretion exist as well [7,9]. However, unlike our study, most of the previous studies were retrospective trials.…”

Section: Discussioncontrasting

confidence: 64%

Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis

Abdel-Raheem

Potti

Tadros

et al. 2002

Pathophysiol Haemos Thromb

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Background: Low-molecular-weight heparins (LMWHs) are being preferred to unfractionated heparin (UFH) because of their superior convenience and a comparable or slightly better toxicity profile. Whether LMWH has an inhibitory effect on aldosterone that causes hyperkalemia is yet uncertain. Methods: Twenty-eight patients (all male; mean age: 70 years, range 52–87 years) placed on LMWH therapy (40 mg subcutaneously every 12 h) for deep venous thrombosis prophylaxis after an operation were included in the study. Transtubular potassium concentration gradient (TTKG) was calculated 1 day prior to LMWH therapy and again after 4 days of treatment. Of the 28 patients enrolled in the study, we were able to calculate the TTKG in only 19 patients: 9 had a urinary osmolarity (either before or after LMWH therapy) less than the serum osmolarity, making the TTKG calculation unreliable. The Wilcoxon signed-rank test was used to analyze differences in the median serum potassium levels and TTKG before and after LMWH therapy. Results: All patients had adequate renal function (creatinine clearance >90 ml/min). Mean (± SD) serum potassium concentration before LMWH was 4.25 (± 0.40) mmol/dl. It increased to 4.35 (± 0.41) mmol/dl after initiating LMWH therapy (p = 0.09). Similarly, the mean (± SD) TKKG calculated was 5.52 (± 2.33) before and 5.97 (± 3.06) after 4 days of LMWH (p = 0.54). Conclusions: Unlike UFH, LMWH (Lovenox^®) in doses used for postoperative prophylaxis against deep venous thrombosis does not seem to have a significant effect on potassium homeostasis.

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“…Heparins inhibit aldosterone synthesis, mainly by reducing the number and affinity of angiotensin II receptors in the adrenal zona glomerulosa, 13 although this effect is not a consistent finding. 14 The inhibitory effect is specific to aldosterone, and other corticosteroids are not affected, although some clinicians recommend that a short tetracosactide (synACTHen) test is done to exclude Addison's disease.…”

Section: Causes Of Type IV Renal Tubular Acidosis Includementioning

confidence: 99%